Allergic airway inflammation is a Th2 driven inflammatory process characterized by excess mucus production, eosinophilia, and airway hyperresponsiveness (AHR). Recent studies have identified that Interferon gamma (IFN-g) plays a critical role in regulating asthmatic response to inhaled allergen by reducing the Th2 effector functions noted above. It also controls airway chitinase activity, a recently characterized pro-inflammatory Th2 effector pathway in asthma. We hope to define the mechanisms by which IFN-g regulates Th2 effector function. In Aim I, we will determine how airway epithelial cells respond to IFN-g to limit Th2 responses, specifically mucus and chitinase activity. In Aim II, we will define the mechanisms by which IFN-g exerts its effects on the Th2 effector cells; acting to increase soluble immunomodulating factors such as IL-13Ra2, decreasing cell surface receptor expression or by affecting post receptor signaling cascades. [unreadable] [unreadable]